Patterns of Expression of Vaginal T-Cell Activation Markers during Estrogen-Maintained Vaginal Candidiasis

Al-Sadeq Ameera, Hamad Mawieh, Abu-Elteen, Abu-Elteen Khaled

Description

The immunosuppressive activity of estrogen was further investigated by assessing the pattern of expression of CD25, CD28, CD69, and CD152 on vaginal T cells during estrogen-maintained vaginal candidiasis. A precipitous and significant decrease in vaginal fungal burden toward the end of week 3 postinfection was concurrent with a significant increase in vaginal lymphocyte numbers. During this period, the percentage of CD3 + , CD3 + CD4 + , CD152 + , and CD28 + vaginal T cells gradually and significantly increased. The percentage of CD3 + and CD3 + CD4 + cells increased from 43% and 15% at day 0 to 77% and 40% at day 28 postinfection. Compared with 29% CD152 + vaginal T cells in naive mice, > 70% of vaginal T cells were CD152 + at day 28 postinfection. In conclusion, estrogen-maintained vaginal candidiasis results in postinfection time-dependent changes in the pattern of expression of CD152, CD28, and other T-cell markers, suggesting that T cells are subject to mixed suppression and activation signals.

Sujets

• CD28
• CTLA-4
• Estrogen
• Candidiasis

Informations

• Publié par: biomed
• Publié le: 01 janvier 2008
• Nombre de lectures: 4
• Langue: English

Extrait

Original article

Patterns of Expression of Vaginal T-Cell Activation Markers during Estrogen-Maintained Vaginal Candidiasis

Ameera Al-Sadeq, MSc, Mawieh Hamad, PhD, and Khaled Abu-Elteen, PhD

thE ImmuNosuppREssIvE àCTIvITy of EsTRoGEN wàs fuRThER INvEsTIGàTEd by àssEssING ThE pàTTERN of ExpREssIoN of cD25, cD28, cD69, àNd cD152 oN vàGINàL t CELLs duRING EsTRoGEN-màINTàINEd vàGINàL CàNdIdIàsIs. a pRECIpITous àNd sIGNIfiCàNT dECREàsE IN vàGINàL fuNGàL buRdEN TowàRd ThE ENd of wEEk 3 posTINfECTIoN wàs CoNCuRRENT wITh à sIGNIfiCàNT INCREàsE IN vàGINàL LymphoCyTE NumbERs. DuRING ThIs + + + + + pERIod, ThE pERCENTàGE of cD3 , cD3 cD4 , cD152 , àNd cD28 vàGINàL t CELLs GRàduàLLy àNd sIGNIfiCàNTLy INCREàsEd. thE pERCENTàGE of + + + + cD3 àNd cD3 cD4 CELLs INCREàsEd fRom 43% àNd 15% àT dày 0 To 77% àNd 40% àT dày 28 posTINfECTIoN. compàREd wITh 29% cD152 + vàGINàL t CELLs IN NàIvE mICE, > 70% of vàGINàL t CELLs wERE cD152 àT dày 28 posTINfECTIoN. iN CoNCLusIoN, EsTRoGEN-màINTàINEd vàGINàL CàNdIdIàsIs REsuLTs IN posTINfECTIoN TImE-dEpENdENT ChàNGEs IN ThE pàTTERN of ExpREssIoN of cD152, cD28, àNd oThER t-CELL màRkERs, suGGEsTING ThàT t CELLs àRE subjECT To mIxEd suppREssIoN àNd àCTIvàTIoN sIGNàLs.

KEy woRds:CD28, CD152, estrogen, vaginal candidiasis, vaginal T lymphocytes

aginal candidiasis (VC) is now recognized as a ma- V jor health problem for women of childbearing age worldwide., The majority of genitourinary tract fungal in- fections are caused byCandida albicans3; VC cases owing toC. glabrata, C. tropicalis,andC. kruziare also on the rise.4, The majority of women who experience sporadic episodes of VC are otherwise healthy. However around 10% of women are at increased risk of VC owing to compromised immunity antibi- otic overuse and increased estrogen concentration in the re- – productive tract environment. 3, Estrogen predisposes to VC by several proposed mechanisms including the enhancement of the pathogenic potential ofCandidaspecies and the sup- – pression of host immunity.  Induction of a pseudoestrous state by estrogen is routinely used to establish experimental – persistentC. albicans4 Fur-vaginal infection in rodents., thermore estrogen administered on a weekly basis can in- duce persistent VC in naive non–germ-free Balb/c mice.3 It is well established now that both innate and acquired

Ameera Al-Sadeq andKhaled Abu-Elteen:of Biology and Department Biotechnology, Hashemite University, Zarqa, Jordan;Mawieh Hamad: Department of Biology and Biotechnology, Hashemite University, Zarqa, Jordan, and Taif University School of Medicine, Taif, Saudi Arabia. is work was funded by research grant MH/02/05 from the School of Graduate Studies and Scientific Research, Hashemite University, Jordan. Correspondence: Mawieh Hamad, PhD, Taif University School of Medicine, Haweyah, Taif, Saudi Arabia; e-mail: [e-mail]. © The Canadian Society of Allergy, Asthma and Clinical Immunology DOI 10.2310/7480.2008.00019

immune responses converge to protect the host against fun- gal infections (reviewed in Romani). Intact epithelia and en- dothelia microbial antagonism and antimicrobial peptides provide the very first line of defense against fungal infections. Additionally professional phagocytic cells (neutrophils monocytes macrophages and dendritic cells [DCs]) reduce fungal burden by inducing oxidative and non-oxidative kill- ing of fungi and by restricting fungal growth and infectivity. Nonetheless localized T cell–mediated immunity (CMI) specifically T-helper (Th)1-mediated responses remains the major defense mechanism against VC., Systemic T-cell re- – sponses generated following the induction of VC  fail to provide significant protection against subsequent localized C. albicansinfection in mice with experimental VC. Dele- + + tion of systemic CD or CD8 T cells does not significantly influence the kinetics of VC in mice. Furthermore absolute numbers of vaginal but not peripheral T cells undergo signif- icant changes during experimental VC in mice. Previously it + has been shown that while CD T cells from draining lymph node and vaginal mucosa undergo minor activation expres- sion of T-cell activation markers α-β7 αM20-β7 and α-β1 drops during primary or secondary estrogen-maintained VC.9 In contrast the expression of mucosal and vascular cell adhesion molecule 1 on vaginal tissue cells is upregulated.9 These findings suggest that despite upregulated expression of several T-cell activation markers during VC lack of expres- sion of corresponding ligands limits the capacity of CMI to deal withC. albicansinfection. Numerous studies vaginal have suggested that CD28/B7 (CD80 or CD86)-dependent T-cell costimulation is essential for induction and mainte-

Allergy, Asthma, and Clinical Immunology, Vol 4, No 4 (Winter), 2008: pp 157–163

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